Prevalent mutations in prostate cancer

被引:151
作者
Dong, JT
机构
[1] Emory Univ, Sch Med, Winship Canc Ctr, Program Genet & Mol Biol,Dept Hematol & Oncol, Atlanta, GA 30322 USA
[2] Emory Univ, Sch Med, Winship Canc Ctr, Program Genet & Mol Biol,Dept Urol, Atlanta, GA 30322 USA
关键词
prostate cancer; tumor suppressor gene; oncogene; mutation; deletion; amplification; haploinsufficiency;
D O I
10.1002/jcb.20696
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Quantitative and structural genetic alterations cause the development and progression of Prostate cancer. A number of genes have been implicated in prostate cancer by genetic alterations and functional consequences of the genetic alterations. These include the ELAC2 (HPC2), MSR1, and RNASEL (HPC1) genes that have germline mutations in familial prostate cancer; AR, ATBF1, EPHB2 (ERK), KLF6, mitochondria DNA, p53, PTEN, and RAS that have somatic mutations in sporadic prostate cancer; AR, BRCA1, BRCA2, CHEK2 (RAD53), CYP17, CYP1B1, CYP3A4, GSTM1, GSTP1, GSTT1, PON1, SRD5A2, and VDR that have germline genetic variants associated with either hereditary and/or sporadic prostate cancer; and ANXA7 (ANX7), KLF5, NKX3-1 (NKX3.1), CDKN1B (p27), and MYC that have genomic copy number changes affecting gene function. More genes relevant to prostate cancer remain to be identified in each of these gene groups. For the genes that have been identified, most need additional genetic, functional, and/or biochemical examination. Identification and characterization of these genes will be a key step for improving the detection and treatment of prostate cancer.
引用
收藏
页码:433 / 447
页数:15
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